{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nMYBL2 (also known as B‐Myb) is a critical, evolutionarily conserved transcription factor that orchestrates normal cell cycle progression. It regulates the timely expression of numerous genes required for the G1/S transition, S‐phase progression, and entry into mitosis. In normal cells, MYBL2 activity is achieved through its dynamic interactions with multiprotein complexes – for example, its assembly with the MuvB core and LIN9 enables activation of G2/M genes, while its association with factors such as MALAT1 influences pre–mRNA processing and alternative splicing of its own transcripts. In addition, MYBL2 plays roles in maintaining cell‐cycle checkpoints and affects cellular senescence through the regulation of key targets (for example, p16^INK4α), thereby underscoring its importance in coordinating cell proliferation and differentiation."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn a wide variety of human malignancies, aberrant up‐regulation and dysregulation of MYBL2 contribute to tumor initiation, progression, and therapeutic resistance. Elevated MYBL2 levels have been observed in cancers such as breast, hepatocellular, lung, gallbladder, and pancreatic adenocarcinomas, as well as in hematological malignancies including acute myeloid leukemia and aggressive neuroblastomas. In these settings, MYBL2 not only drives the expression of genes required for cell proliferation and mitosis but is also subject to regulation by microRNAs (for example, miR‐29, miR‐30, and miR‐143) and noncoding RNAs (including MALAT1 and circular RNA isoforms) that modulate its mRNA stability, alternative splicing, and post–translational activation (via sequential phosphorylation and protein complex remodeling). Moreover, oncogenic signals—such as those emanating from MYCN amplification, human papillomavirus E7, or disrupted pVHL function—can engage MYBL2 in positive feedback loops that further enhance its ability to activate cell cycle programs and override cell cycle checkpoints. These multifaceted regulatory mechanisms, uncovered in studies spanning cervical, endometrial, glioma, and bladder cancers among others, support the emerging view of MYBL2 as a pivotal mediator of tumor cell proliferation, invasiveness, and chemoresistance, as well as a promising therapeutic target."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "37"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Giorgia Santilli, Rebekka Schwab, Roger Watson, et al. 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